Lyme Disease Support Group

Herb; Cats Claw, uncaria tomentosa

This herb (inner bark) is an immune potentiator, anti-inflammatory, analgesic that has positive features for chronic Lyme infections that have become both immune disabling and brain central nervous system conditions.

Herb;  Sarsaparilla; smilax glabra officinalis

This remarkable herbal (root) has a history in treatment of syphilis infections.  It is antibiotic, anti-spirochete and immune system modulating which means it is selective in stimulating good immune response and dampening imbalanced responses. 

Herb; Andrographis (andrographis paniculata)

This herbal substance and its extracts in its effects is anti-inflammatory, analgesic, anti-bacterial, anti-viral and very importantly “anti-spirochetal”.  This is useful specifically because Lyme type bacteria are spirochetes.

The Lyme type spirochete is anaerobic or oxygen avoidant.  That is one of its most basic characteristics as a living organism.  As that cannot be changed it also offers something that can be used in treatment.  This was recognized early by various physicians who attempted to exploit this natural vulnerability.  They tried to kill the infective bacteria by using hyperbaric oxygen chambers.  They placed patients in these oxygen chambers in hopes that volume oxygen would irradiate infections.  Yet after many sessions of oxygen chamber therapy, it was apparent this treatment failed.

"Corticosteroids, or steroids as they are commonly called, are very important drugs in a wide variety of medical conditions.  They exert an  anti-inflammatory  effect and suppress the immune system.  This may be life saving in some diseases such as asthma and malignancies. 

On the  other hand, steroids are rarely curative, and are associated with harmful side effects if used for prolonged periods of time.  These include:

please go to:

 http://www.mdjunction.com/forums/lyme-disease-support-forums/studies-research/10292364-tom-griers-observations-cdcnih-webinar-on-ld-testing

when owner, roy, posted this article here,  ALL paragraph spacings were LOST!  below is one long paragraph that was NOT submitted that way.

 bettyg, iowa

IgM = Early antibodies produced in new infections. IgM can rise and fall as infection wax and wane.

IgG = Late antibody that is more specific to the infection but take 4-6 weeks to be produced.

Awhile back I viewed the taxpayer paid CDC webinar October 1st, 2012 on Lyme disease testing and future research directions.

I was quite disappointed at both the direction of research and the analysis of current testing. http://www.cdc.gov/lyme/diagnosistreatment/index.html

RF = Relapsing Fever

In late 19th century Germany, there was a epidemic febrile disease whose hallmark symptoms included fevers that recurred approximately every few weeks.

In 1868, Dr. Otto Obermeier isolated the organism from sick patients; a bacterium now known as Borrelia recurrentis.

Then in 1874, Dr Gregor Munch injected himself with the suspected pathogen. Dr. Munch not only became quite ill, but he experienced several feverish relapses.

His experiment thus proved that Borrelia species was the culprit that was causing the German epidemic of recurring fevers.

Later French researchers Sergent and Foley identified the human-louse as the vector of the disease.

The concept that Relapsing Fevers were only transmitted by human lice, was about to be shattered.

Definitions

Substrate Drugs -

Drugs that are acted upon by the liver cytochrome enzymes and partly or entirely metabolized by the cytochrome enzymes, these drugs compete with each other to be metabolized at the same sites in the liver.

Cytochrome Inhibitors -

Any medication that suppresses the action of, or blocks the cytochrome enzymes.

These drugs can also be substrate drugs, and suppress metabolism that leads to increased blood levels of p450 substrate medications.

Dear Doctor Aronowitz,

I have been an advocate of better science in Lyme disease research since 1990 when I was then misdiagnosed by the Lyme experts with Multiple Sclerosis.

Since then I have fought with everything I have for pathology and autopsy data to establish whether Borrelia bacteria can persist within the human brain post antibiotic treatment.

I've had several people ask me recently where my full story is.  I suppose I've kind of been avoiding it because it's difficult to know where it begins, and it certainly hasn't ended.  See, I've come to the realization that Lyme disease is not just the process of being infected, being properly diagnosed (or not), and being treated.  It is much more complex than that.  It is a stealthy and highly evolved bacterium that affects every person differently and to different degrees.

The severity of the infection is dependent on the presence of other co-infections or other underlying conditions such as genetics, the strength of your immune system, your diet, your mindset, your social and emotional well-being, stress levels, companionship, the list goes on.  It is dependent on each individual person and their overall health.  How it affects one person can be completely different from the next.  Some people can harbor Lyme and not have symptoms for years, until the circumstances are just right.  That's what happened to me.

 Like many who had Chronic Lyme disease I went through a tremendous amount of hassle and frustration, clueless doctors, misinformation, massive doses of antibiotics that did nothing, new age cures that did not work, the loss of energy, and chronic pain.  As a result of all of this I sunk into a major depression.   Before I was bitten by that deer tick I had a solid meditation practice and in the end this is what literally saved my life.  (You can see my profile for more details).  What I learned from all this frustration was that, if I was going to do the impossible and heal from Lyme, I was going to have to listen closely to my body and become more self reliant.  I was lucky in that I found a doctor who gave me the suggestion to try the Cowden Protocol.  I only had one appointment with him but he pointed me in the right direction.  The Cowden Protocol relies on natural herbal antibiotics along with strict diet restrictions and a keen self awareness.

The association of time to allergic cycles and the purposed or circumstantial exposures that I have experienced may hold some importance.  I wanted to share some anecdotal facts that are possibly of significance in my personal experience of infection.

I hope this paper is informative to the new Lyme patient introducing not just the history of Lyme disease, but also the source and continuation of the controversies and confusion about persistent Lyme disease,

Truth and Consequences (part 1)

MAY 2011

By Tom Grier

May is National Lyme Disease Awareness Month: To introduce lay people and newly diagnosed Lyme patients to the complexities and the controversies of Lyme disease I have rewritten a paper I wrote 13 years ago to reflect a few of the things that we have learned about Lyme disease since 1997.

I am sorry to say that it is too little and not enough, and that the battle to better understand this disease still rages on.

We absolutely need better pathology studies to show without question that Borreliosis can be and often is despite antibiotic treatments, a persistent and incurable infection.

Furthermore, it is a disease that can infect and affect many organs and tissues. But perhaps worst of all is the medical community’s inability to grasp or believe that the Lyme spirochete can and does infect, inhabit, and impair the human brain.

Tom Grier

This paper was written to outline some of the problems associated with the diagnosis of Lyme disease. It turned out much longer than expected.

The paper has been broken up into brief sections. A two page summary is available. Link to two page summary

http://lyme.kaiserpapers.org/20-reasons-why-lyme-disease-is- undiagnosed-summary.html

20 Reasons Why Lyme Disease Is Underdiagnosed –

Summary

Miguel Perez-Lizano, June 2010

Note to Reader;

Lyme disease may well be the most underdiagnosed medical condition in the United States. Some reasons for this are given below.

Many are related to monetary considerations. Supporting detail for these reasons is given in the full version of this document. Link to full version URL (is at end of this long post).

Extremely poor “screening” test

The ELISA screening test recommended by the CDC is, at best, poor, failing to detect 50% or more of Lyme disease cases even under optimal conditions. Strain variations complicate testing.

The unsatisfactory state of Lyme disease testing prompted a U.S Senate directive in Public Law 107-116 signed in 2002. “The Committee recognizes that the current state of laboratory testing for Lyme disease is very poor." The CDC and FDA were instructed to develop accurate tests.

No standard presentation of Lyme disease

Lyme disease can present in a variety of ways. The result is that it can be misdiagnosed as fibromyalgia, MS, Parkinson’s, CFS, Lou Gehrig’s, arthritis, cardiac problems, Alzheimer’s, ADD, vision and hearing problems, and other conditions, including psychiatric disorders.

Highly restrictive CDC surveillance criteria

For surveillance purposes, the CDC has issued serodiagnostic criteria to include only “certain” cases of Lyme disease.

Perhaps fewer than 5% or 10% of proven Lyme disease cases can meet these criteria.

Laboratories are forced to report results as “positive” or “negative” depending on whether they meet the CDC surveillance case definition. Uninformed doctors mistake the CDC case definition as diagnostic criteria.

Misleading implications of low “reported” cases

In addition to CDC surveillance criteria causing very low numbers of reported cases, most state health agencies are not well informed and may not report Lyme disease for various reasons, including the disease may have been acquired elsewhere.

Most doctors mistakenly interpret low or no reported figures to mean Lyme disease in their state is rare or absent.

Lack of reliable tick and tick borne disease studies

Tick studies outside of recognized endemic areas are few and tend to be outdated or badly executed. Hence, tick borne diseases tend to be ignored in areas not recognized to be endemic.

The Infectious Diseases Society of America (IDSA)

The IDSA Lyme guidelines are issued by a few individuals who have blatant conflicts of interest and present flawed and biased information.

These guidelines, the subject of an antitrust investigation, are used by most doctors because they are heavily publicized.

The IDSA, with CDC backing, is the entity most responsible for the unhealthy state of affairs in Lyme disease.

The Centers for Disease Control

Employees at the CDC have their own conflicts of interest regarding Lyme disease. Mostly, these have to do with financial interests in tests and vaccines.

The IDSA appears to be a dominant influence on the CDC which promotes the IDSA Lyme disease guidelines.

Potential expense to HMO’s and insurers

The IDSA/CDC limited definition of Lyme disease, restrictive serodiagnostic criteria, limited treatment approach, and denial that Lyme disease can be a chronic infection are embraced by HMO’s and medical insurers to minimize risk of potential expenses.

Medical conformance enforcement and licensure threats

There are numerous cases of harassment against physicians who treat Lyme disease outside of IDSA guidelines. Many IDSA authors have testified against these physicians. Some states have adopted legislation to prevent this abuse. Many doctors will not help Lyme disease victims.

The media’s role in promoting public and medical ignorance

Rarely do the media question the CDC/IDSA Lyme disease information. They simply parrot and disseminate this information to the unsuspecting consumer, including doctors.

Pharmaceutical windfalls

Symptomatic treatment of undiagnosed Lyme disease is a financial bonanza for drug companies.

The research racket

Research funding for Lyme disease has been concentrated to a favored few mainly connected with IDSA. One result is that the research has been biased.

Test and vaccine patents

The number of patents related to Lyme disease has dwarfed those of diseases that Lyme disease can mimic, such as MS or Parkinson’s disease.

Lack of significant scientific progress in Lyme disease may be partially explained by the protection of monetary turf by these patent holders.

Medical testing laboratories

The IDSA/CDC two-tier test approach, a positive ELISA followed by Western Blots, is a financial windfall to testing laboratories and test patent holders but a detriment to diagnosis.

Potential impact on disease charities

Disease charities built around diseases that can be misdiagnosed Lyme disease amount to many hundreds of millions of dollars.

If a substantial number of these diseases were found to be misdiagnosed Lyme disease, revenues for these specialized charities would likely suffer.

Potential impact on specialty diseases doctors

The impact would be the same as for disease charities on the income of these specialized doctors.

Potential impact on disability payments

Appropriate recognition of the prevalence and disabling aspects of Lyme disease could place a large burden on disability payments.

Potential impact on tourism and real estate prices

Tourism agencies and real estate professionals prefer to minimize the prevalence of Lyme disease.

Potential employer liabilities

Employers prefer that Lyme disease not be recognized either as a geographic threat or a serious health threat. This is particularly true for those who employ outdoor workers.

Biowarfare aspects

Some knowledgeable observers have suggested that biowarfare is an important contributor to the poor state of affairs in Lyme disease, including the lack of quick and reliable diagnostic methods and lack of a cure.

There is no doubt that Lyme disease is being studied for biowarfare.

lyme.kaiserpapers..org

KaiserPapers.org In Copyright since 2000

Tomgrier2001@yahoo.com

We have talked about how the Lyme spirochete attaches to the endothelial cells in blood vessels, and creates “LEAKY” blood vessels. Due to the spirochete’s exceptional motility, this allows the bacteria to enter virtually any tissue in the human body.

The big questions are: Where is it going? Why does it want to go to specific places? What happens when it gets to places where it can hide and survive?

Bacteria don’t have brains, but they do have millions of years of evolution that improved their overall survival through shear trial and error. The bacteria wants to survive.

For good or bad Borrelia bacteria have made their homes in ticks and mammals. How has evolution affected their genetics in order to enhance their own survival in ticks and mammals?

Let’s look at Borrelia bacteria from the bacterium’s point of view.

All known species of Borrelia bacteria that cause Relapsing Fever and Lyme Disease enter the blood of humans either by way of an insect bite such as from an infected tick, head-lice, or through infected blood contact.

Relapsing Fever caused by Borrelia recurrentis enters the blood stream through open bleeding capillaries on the head caused by the host scratching at lice and themselves until they are bloody, and then accidentally crushing the head-louse allowing the bacteria direct entry into the blood stream.

Dr. Joseph Dutton was infected with Borrelia duttonii when he was performing an autopsy on an African native who died very quickly of neuroborreliosis-encephalitis after contracting Relapsing Fever through the bite of the moubatta tick.

Unfortunately Dr. Dutton cut himself during this field autopsy, was also infected, and died of encephalitis within two weeks of initial infection.

Below is an excerpt from Dr. Willy Burgdorfer’s lecture on the history of spirochetes related to Lyme disease.

Take special note about the disappearance of classical formed spiral spirochetes in favor of granular-cysts, and also the ability of Borrelia to invade epithelial cells and appear to have disappeared.

This is a history and research that we cannot ignore and cannot afford to forget.

If we had looked at this evidence in 1982, we would have understood the paradoxes we were seeing and incorrectly dismissing as artifacts, in our diagnosis, treatment, and relapses of Lyme patients.

At the turn of the century, 1903 through 1905, the British physicians Dutton (Joseph Everett) and Todd (John Lancelot) working in the Congo, found that the disease referred to as "human tick disease" by David Livingston as early as 1857, was caused by a spirochete transmitted by the African soft-shelled or argasid tick, Orhithodoros moubata (Fig. 3).

Both Dutton and Todd contracted the disease.

Dutton, a pathologist, infected himself accidentally during a post mortem and died.

He is remembered by having had named the East African relapsing fever spirochete Borrelia duttonii.

Also playing an important role in relapsing fever research was the German microbiologist Robert Koch.

At the end of 1904, he was called to East Africa to investigate the widely distributed East Coast Fever in cattle.

He soon learned that most Europeans traveling into the interior regions had been suffering of recurrent fever first thought to be malaria.

Although Koch was not aware of the British findings in the Congo and Uganda, he confirmed the vector role of the Orhithodoros moubata.

He was the first to demonstrate that spirochetes were transmitted via eggs (transovarial transmission) to the progeny of infected female ticks.

Ever since it was demonstrated that the body louse (Pediculus humanus humanus) and the African O moubata were the vectors of the relapsing fever spirochetes known today as Borrelia recurrentis and B duttonii, respectively, intense studies have been carried out on the development of these microorganisms in their vectors, and on the mode of transmission to humans.

full part 3-A can be found here:

http://www.mdjunction.com/forums/lyme-disease-support-forums/studies-research/1840726-part-2-lyme-on-the-brain-by-tom-grier-82210

Part 4

Lyme on the Brain

Lecture Notes by Tom Grier

August 28, 2010

tomgrier2001@yahoo.com

218-728-3914

If we look back and do a quick review of the lecture so far, we see some important points that keep repeating themselves in all stages and aspects of Lyme disease.

This is because of their fundamental importance in the disease process. To understand and make sense of the end stages of Lyme disease, we have to understand the fundamentals.

Lyme on the Brain - Part 1

1) Lyme was first misdiagnosed as Juvenile Rheumatoid Arthritis in Old Lyme, Connecticut.

2) In 1975, Lyme disease was first described in print as primarily an arthritic disorder.

4) This treatment protocol was initiated seven years before we knew that the actual cause of Lyme disease was caused by a spirochetal bacterium.

5) Lyme disease is caused by a spirochete in the same Genus as Tick-Born Relapsing Fever (Borrelia) a genus with tremendous variation.

6) Spirochetes are known to persist, and cause relapses.

7) Borrelia can change forms from spirals to cysts, and can change their surface antigens quickly.

Part 2

1) The Lyme spirochete attaches to blood vessels and causes leaks to occur.

Once the BBB closes, it sequesters the infection inside the brain away from the immune system and treatment.

3) Borrelia can have many strain variations and can adapt and change quickly.

4) The current Lyme serology tests that use strain B-31 are not representative of the wild strains found in nature. (Dr. Ron Shell, Madison, Wisconsin).

5) The new Western Blot Reporting criteria or Dressler Criteria turns a poor test into a nearly worthless test. Two-tiered testing further makes Lyme disease diagnosis less accurate.

6) Lyme bacteria can enter the blood vessel endothelial cells, and evade the immune system. (Sturrock and Ma).

7) Antibiotic treatment failure has been documented since 1979, and seven antibiotic treatment studies all demonstrated antibiotic failure ranging from 25% to 50%.

Part 3

1) Lyme disease is part of a larger pandemic called: Relapsing Fever.

2) Neurogenic strains of Relapsing Fevers go to the brain and are deadly.

3) The Lyme bacteria can hide inside cells (fibroblasts, endothelial cells) and seeks tissues where it is protected from oxygen and the immune system.

4) Bb often hides inside connective tissue like tendons and the joints; Bb especially seeks the brain as prime target tissue.

5) There has been an extensive history of [b]over 50 medical articles of spirochetes as one possible cause of MS published since 1911 in prestigious medical journals.

6) Dr. Gabriel Steiner demonstrated classical form spirochetes in MS patients in Germany since 1922, and again in Michigan MS patients in 1952. [/b]

7) In 1957, Dr. Rachael Ichelson, in Philadelphia, demonstrated spirochetes in MS patients and developed a culture technique to detect them.

8) Dr. Patricia Coyle tests 47 MS patients with an antigen/antibody complex test and finds that 15 of 47 MS patients have Lyme and respond to antibiotics, this refutes her prior published study where 20 random MS patients received an ELISA test and all tested negative. But her new 47 patient study was NEVER published.

Part 3-B continued

LYME ON THE BRAIN by Tom Grier, 8.28.10

Also in modern Lyme disease mouse model; the infection appears to have disappeared, but ticks that feed on the mice can then infect other mice. We might be looking for spirals, but that doesn’t mean that’s what we will find in every case.

Spirochetes are masters at morphing and changing forms. It helps them survive or another way of putting it; it contributes to relapses occurring even after aggressive antibiotic therapy.

What these early MS researchers found was amazing.

First most isolated the bacteria from the human MS lesions, but just like Syphilis, they found it was only possible to keep them alive in animal models.

Culturing Borrelia in 1911 was just not yet possible.

Once the organism was introduced to various animal models, it was often and many times re-isolated from the brains of the animals and reintroduced to new uninfected animals with exactly the same results.

The bacteria found its way to the brain of the animals, and the brain tissue could cause infection in uninfected animals.

The research became so established that the researchers often communicated with each other and commonly referred to the organism as “The MS Spirochete” which was eventually named Myela phethora or “myelin loving” by Dr. Gabriel Steiner from Germany.

Steiner transferred the MS agent to many animals including monkeys. He created a better silver-stain, which we still use, today and is called Steiner-Silver-Stain.

When things got dicey for Jewish scientists in Germany in the mid 1930s, Steiner fled Germany and resettled in Ann Arbor, Michigan.

Steiner did not publish again for over a decade, and was amazed that America had nearly no knowledge of the European spirochete model of MS, so he wrote an article in 1952 called: “The Pathogenic Role of Spirochetes in the Etiology of Acute Plaques in MS”.

What Steiner found in American MS patients was the same as other parts of the world. MS lesions sometimes contained spirochetes that could infect animal models.

Compare below the photo of a spirochete from the lesion of a German MS patient in 1922, compared to the spirochete isolated from an American MS patient in 1952 from Michigan.

His work was completely corroborated by an American scientist Dr. Rachael Ichelson, who worked in public health in Philadelphia for 40 years.

Lyme Lecture Outline Notes

Hi, I promised Wisconsin’s Mike N., I would try and post some of my lecture notes from August 5th without the slides.

Here is part 1 of 4 from recent August 2010, Amery and Hayward, Wisconsin talks called Lyme On The Brain.

Tom Grier tomgrier2001@ yahoo.com

Introduction

Lyme disease was first recognized in Old Lyme, Connecticut, CT, in 1973 by two concerned mothers.

Judy Mensch and Polly Murray felt there were too many diagnosed cases of Juvenile Rheumatoid Arthritis in their neighborhood children.

Judy and Polly Murray who had backgrounds in public health collected over 200 local case histories and presented them to the CDC and CT health department.

Dr. Alan Steere, MD investigated the local cases of JRA and coined the misnomer "Lyme Arthritis" in his 1975 publication that first described Lyme Borreliosis as an arthritic disorder.

Although the actual cause of Lyme arthritis that was sometimes associated with a bull's-eye rash was not yet known, a treatment protocol of two weeks of tetracycline was already being recommended.

The infectious etiology of Lyme disease was not known until 1981 when Dr. Willy Burgdorfer, PhD from Rocky Mountain Labs in Colorado isolated the new species of Borrelia bacteria from a tick from Shelter Island.

The fact that "Lyme disease" was caused by a spirochete should have been a real concern and everything we thought we knew about Lyme disease should have been reevaluated at that time.

Borrelia was a family of bacteria not only associated with relapses and antibiotic treatment failures, but also is part of the same family of bacteria that causes [b]Tick-Borne Relapsing Fevers, a group of over 300 variant diseases that can be deadly within months:[/b]

(Borrelia duttonii and Borrelia crocidurai of Northeast Africa), or considered mild and often mislabeled as "self-limiting"; such as, Borrelia recurrentis found in the Southwest USA.

(Ron Ferris of Canada was diagnosed with Borrelia recurrentis and was sick for years despite treatment right up until the day he died).

In 1982 the Lyme bacteria was isolated from the "Lyme Bull's-Eye rash" from patients from New England.

With this new discovery causing so much excitement and demanding large sums of monies to investigate, no one wanted to admit that "Lyme" was just a new subclass of a larger world-wide disease spread by ticks that was well known for a century as tick-born-relapsing fevers.

We need to stop calling this disease Lyme disease and recognize that it is part of a worldwide problem called Borreliosis.

The heart and soul of the mechanism of infection, or the pathogenesis of Borrelia bacteria that cause Relapsing Fever and Lyme disease is its ability to attach to the lining of blood vessels and cause gaps or holes to appear between the endothelial cells.

The endothelial cells themselves release digestive substances, as well as our own white blood cells releasing blood-born immune factors such as tissue plasminogen, TNF-alpha, IL-1, Il-6, histamines, vaso-active amines and MMP-9 that facilitates cell penetration through any and all blood vessels, but especially important is the immediate transit of Borrelia burgdorferi through the blood-brain-barrier.

Animal models including dogs and primates show conclusively that this is not just a random occurrence, but rather a very specific mechanism that facilitates both the immediate and long-term survival of Borrelia within mammalian systems.

In dog-models, the uninfected dog’s blood protein albumin was tagged with radioactive Iodine, and then traced using radio-detection of entering the brain and spinal-fluid. After infected ticks were allowed to feed on the dogs, this “leaky-brain-effect” took less than 24-48 hours to reach its full potential.

We can measure and observe this leaky-brain-effect in dogs, hamsters, rabbits, and primates within hours, and we can see and detect in many other animal models including guinea pigs, mice, hamsters, and rabbits the actual transit of Borrelia into the brain of these animals within days of tick-bite, yet our own USA health-care experts are saying without equivocation that infected ticks have to be attached for at least 36-48 hours.

(YALE Medical Report, IDSA-Lyme Treatment Guidelines)

Why is there such an absolute dictatorship in our guidelines when we have direct animal studies since 1989 that suggest that not only does Borrelia bacteria penetrate blood vessels and enter the brain, but once the blood-brain-barrier closes up 10-14 days after initial infection; the sequester bacterial infection within the brain is undetectable by serology tests.

Our current serology tests that detect antibodies to the Lyme bacteria; require at least 4-6 weeks after exposure to produce significant antibodies to the Lyme bacterium.

By then the infection can be resting dormant and quiescently within the host’s brain, undetected, undetectable, and creating changes within the brain that are subtle and perhaps for awhile negligible.

Published in Volume 119, Issue 12 (December 1, 2009)

J Clin Invest. 2009;119(12):3652–3665. doi:10.1172/JCI39401.

Copyright © 2009, American Society for Clinical Investigation

Research Article

Live imaging reveals a biphasic mode of dissemination of Borrelia burgdorferi within ticks

Star M. Dunham-Ems1,

Melissa J. Caimano1,

Utpal Pal2,3,

Charles W. Wolgemuth4,5,

Christian H. Eggers6,

Anamaria Balic7 and

Justin D. Radolf1,8

1Department of Medicine, University of Connecticut Health Center, Farmington, Connecticut, USA.

2Department of Veterinary Medicine, University of Maryland, College Park, Maryland, USA.

3Virginia-Maryland Regional College of Veterinary Medicine, College Park, Maryland, USA.

4Department of Cell Biology and

5Center for Cell Analysis and Modeling, University of Connecticut Health Center, Farmington, Connecticut, USA.

6Department of Biomedical Sciences, Quinnipiac University, Hamden, Connecticut, USA.

7Department of Craniofacial Sciences and

8Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, Connecticut, USA.

Address correspondence to:

Justin D. Radolf,

Department of Medicine,

University of Connecticut Health Center,

263 Farmington Avenue,

Farmington, Connecticut 06030-3715, USA.

Phone: (860) 679-8480; Fax: (860) 679-1358;

E-mail: jradolf@up.uchc.edu.

First published November 16, 2009

Received for publication April 1, 2009, and accepted in revised form September 30, 2009.

Lyme disease is caused by transmission of the spirochete Borrelia burgdorferi from ticks to humans.

Although much is known about B. burgdorferi replication, the routes and mechanisms by which it disseminates within the tick remain unclear.

To better understand this process, we imaged live, infectious B. burgdorferi expressing a stably integrated, constitutively expressed GFP reporter.

Using isolated tick midguts and salivary glands, we observed B. burgdorferi progress through the feeding tick via what we believe to be a novel, biphasic mode of dissemination.

In the first phase, replicating spirochetes, positioned at varying depths throughout the midgut at the onset of feeding, formed networks of nonmotile organisms that advanced toward the basolateral surface of the epithelium while adhering to differentiating, hypertrophying, and detaching epithelial cells.

In the second phase of dissemination, the nonmotile spirochetes transitioned into motile organisms that penetrated the basement membrane and entered the hemocoel, then migrated to and entered the salivary glands.

We designated the first phase of dissemination “adherence-mediated migration” and provided evidence that it involves the inhibition of spirochete motility by one or more diffusible factors elaborated by the feeding tick midgut.

Our studies, which we believe are the first to relate the transmission dynamics of spirochetes to the complex morphological and developmental changes that the midgut and salivary glands undergo during engorgement, challenge the conventional viewpoint that dissemination of Lyme disease–causing spirochetes within ticks is exclusively motility driven.

has 90-94 references which willy burgdorfer's name shows up and EACH reference is hyperlinked so you click to go to ACTUAL REFERENCE these people found their information; very impressive!

 http://tinyurl.com/2bb2mqw  

bettyg, iowa activist/group leader

Objective: A structured clinical interview is proposed to assist in the overall clinical assessment when late state Lyme disease is suspected.

Method: From a combination of clinical experience, journal review, and discussion with colleagues, a structured interview was developed.

Information from patients with late stage neuropsychiatric Lyme disease (NPLD) was entered into a database to serve as a reference point for diagnosis and tracking the patient’s status after diagnosis.

Details are provided in the text of this article.

Conclusion: When NPLD is a diagnostic possibility, a detailed, well-focused interview and mental status exam is proposed, and a database of symptoms seen in NPLD is established.

It is recommended to continue perfecting the assessment as well as expanding the database.

If diagnostic accuracy is improved, there would be better consensus regarding treatment strategies.

Objective

to read full article click on

http://www.mdjunction.com/forums/lyme-disease-support-forums/studies-research/1749150-neuropsychiatric-assessment-of-lyme-disease

15 May 2010

* Antibodies are in immune complexes

* Spirochete encapsulated by host tissue (i.e.: lymphocytic cell walls)

* Spirochete is deep in host tissue (i.e.: fibroblasts, neurons, etc.)

* Blebs in body fluid, no whole organisms needed for PCR

* No spirochetes in body fluid on day of test

* Genetic heterogeneity (300 strains, 100 in U.S.)

* Antigenic variability

* Surface antigens change with temperature

* Utilization of host protease instead of microbial protease

* Spirochete in dormancy phase (L-form) with no cell walls

* Recent antibiotic treatment

* Recent anti-inflammatory treatment

* Concomitant infection with babesia may cause immunosuppression

* Other causes of immunosuppression

* Lab with poor technical capability for Lyme disease

* Lab tests not standardized for late stage disease

* Lab tests labeled "for investigational use only"

* CDC criteria is epidemiological not a diagnostic criteria

* Lack of standardized control

* Most controls use only a few strains as reference point

* Few organisms are sometimes present

* Encapsulated by glycoprotein "S-layer" which impairs immune recognition

* "S"- layer binds to IgM

* Immune deficiency

* Possible down regulation of immune system by cytokines

* Revised W.B. criteria fails to include most significant antigens

http://flash.lymenet.org/ubb/ultimatebb.php/topic/1/94462

Abstract

A tick-borne, multisystemic disease, Lyme borreliosis caused by the spirochete Borrelia burgdorferi has grown into a major public health problem during the last 10 years.

The primary treatment for chronic Lyme disease is administration of various antibiotics.

However, relapse often occurs when antibiotic treatment is discontinued.

One possible explanation for this is that B. burgdorferi become resistant to antibiotic treatment, by converting from their vegetative spirochete form into different round bodies and/or into biofilmlike colonies.

There is an urgent need to find novel therapeutic agents that can eliminate all these different morphologies of B. burgdorferi.

In this study, two herbal extracts, Samento and Banderol, as well as doxycycline (one of the primary antibiotics for Lyme disease treatment) were tested for their in vitro effectiveness on several of the different morphological forms of B. burgdorferi (spirochetes, round bodies, and biofilmlike colonies) using fluorescent, darkfield microscopic, and BacLight viability staining methods.

Our results demonstrated that both herbal agents, but not doxycycline, had very significant effects on all forms of B. burgdorferi, especially when used in combination, suggesting that herbal agents could provide an effective therapeutic approach for Lyme disease patients.

But it's Bjarnsholt's latest discovery that reveals microbes' gift for language: the bacteria aren't just talking amongst themselves, but also quietly listening in on signals sent by their human host

http://www.newscientist.com/article/mg20527501.300-bugging-bugs-learning-to-speak-microbe.html

Why Lyme Treatments Fail

By James Schaller, M.D., M.A.R.

My average patient has been to 10-50 physicians before me. Such

patients have not been healed of their Lyme disease. Below are

some common reasons for their treatment failure:

They say it is either “negative” or “positive.” Wrong. If a

person has one "fingerprint band”, they have Lyme disease.

These highly specific bands, widely accepted in the world

literature, are 13, 14, 17, 21, 23, 24, 25, 28, 31, 34, 35, 37, 39,

47, 50, 54, 83, 84, 93 and 94. The lab can be a junk lab that

invests nothing to optimize their testing kit, but if one of these

bands is positive—Lyme is present. IGeneX has the best

Western Blot in the world. No other lab has invested so much,

for so long, to create the best test. If your clinician wants to

first use an ELISA, simply run. To put it bluntly, the ELISA

test as a screening tool is useless, missing even the most

obvious PCR positive patients with clear past histories of

massive Bull’s Eye rashes, which, while not the norm, provide

"Tick-borne Disease Research Area - Please Do Not Enter," the sign says on the front door of Kerry Clark's University of North Florida office.

If that's not enough of a deterrence, there are always the photographs of Florida's three most common tick species blown up to larger-than-life proportions

Great article from "Lyme Times" on dealing with kids who have Lyme in school.

Tells you your rights and how to help school staff and teachers!

MICHAEL J FOX ,LYME & PARKINSON'S

Posted By: Daystar <Send E-Mail>
Date: Monday, 16 May 2005, 12:48 p.m.

In Response To: Reader: GRAVIOLA and PARKINSON'S (hobie)

: Michael J Fox has had Lyme Disease. Lyme causes many neurological symptoms and has been linked to Lyme...just like M.S, ALS, Lupus, Alzheimer's, CFS. FM, Normal Pressure Hydrocephalus, etc.

The following is a discussion concerning Fox and his Lyme Disease

Many who first have lyme end up being diagnosed with these other diseases

MJF and Lyme disease - 1997
This article submitted by Art Doherty on 12/1/98.
Email Address: doherty@utech.net

On the cover of the National Examiner's (yes the tabloid) May 27, 1997
edition which is currently out, the "Bug Bite Threatens Michael J. Fox
Career" banner is flying just above "Oprah's Battle With Baldness."
Open to page 35.
Star refuses to take doctors advice to slow down...
MICHAEL J. FOX CAREER THREATENED BY BIZARRE DISEASE.

His nightmare began with a bite from this
little tick! 

ADHD misdiagnosis

LEE COUNTY: Every year, millions of children are medicated for Attention Deficit Hyperactivity Disorder, but a local doctor says they could be misdiagnosed and taking drugs they don't need.

"He was such a good kid. So calm, so laid back, never argued," said Jenny Miner.

That's how Kenny Standish was before kindergarten.

Then he changed.

by Sandra L. Bushmich, MS, DVM
Associate Professor of Pathobiology
University of Connecticut, Storrs, CT 06269

About the Marshall Protocol

The Marshall Protocol is a medical treatment being used by physicians worldwide to treat a variety of chronic inflammatory and autoimmune diseases including (but not limited to) sarcoidosis, Chronic Fatigue Syndrome, fibromyalgia, Crohn’s Disease, and rheumatoid arthritis. While other treatments for chronic disease use palliative medications in an effort to cover up symptoms, the Marshall Protocol is a curative treatment, which strives to address the root cause of the disease process.

Information about the treatment can be found at the study site, marshallprotocol.com and also at autoimmunityresearch.org. The site is run by the staff of the Autoimmunity Research Foundation, a California-based non-profit agency. Over 200 health professionals are members of the site, and discussions are moderated by a group of volunteer nurses. There is no charge to use the website or the treatment and all patients are welcome to participate.

 Tues Mar 3 2009

This story is very similar to Lyme disease's in the essense that the patients spend sometimes a lifetime going from doc to doc... Many think it is Lyme related and there is alot of other information out there about the connection...

(NaturalNews) It sounds like something from a bad sci-fi movie. People report the sensation of creatures crawling under their skin, mysterious moving fibers appear, and finally bugs and worms pop out. Unfortunately, these terrifying symptoms are all too true. The people having them are experiencing Morgellons, the latest and scariest in the series of bizarre diseases appearing in the last few years, seemingly from nowhere. Morgellons is now reaching epidemic proportions in the U.S. and abroad.

Morgellons is a multi-dimensional disease

Morgellons starts with relentless itching, stinging or biting sensations. Cotton-like balls may appear on the body with no reasonable explanation. Soon skin rash develops along with lesions that will not heal. Many sufferers report string-like fibers of varying color popping out through the skin lesions. These fibers can be black, white, red or even iridescent blue. Others report black specks falling from their bodies that litter their sheets and bathrooms. Eventually a variety of bugs and worms begin to find their way out of the body through the lesions. Other accompanying symptoms include hair loss, debilitating and chronic fatigue, hard nodules beneath the skin, and joint pain.

Morgellons also has a cognitive aspect. People with the disease experience neurological damage that manifests as difficulty concentrating, inability to process and use language effectively, and generalized brain fog. The presence of reduced cognitive ability has made it easier for doctors to dismiss Morgellons and send patients away with a diagnosis of delusional parasitosis, meaning they are imagining they are infected by parasites. After the typical eight minute visit, traditional doctors pull out their prescription pads and write these people prescriptions for antidepressants or antipsychotic medications.

As a result, Morgellons also has a psychological component. Once people become aware that symptoms such as theirs are treated as delusions they are reluctant to seek further medical attention and tend to withdraw from society with their only contact with others being through the internet. They begin living the lifestyle of the leper. Many have to give up their jobs and become dependent on public assistance. This adds to the psychological debilitation of the disease. Not being taken seriously when you know you have a terrifying and devastating disease causes permanent psychological damage.

Member 'LDSUCS' has been through alot and she gave me permission to share her story

 My daughter got Lyme from me via pregnancy. I went into preterm and gained 100 pounds of mostly fluid mix with fat...I was a swollen ball. My feet were so big no shoes could fit me and this was after the delivery...I got so much worse after the pregnancy. I didn't know I had Lyme. I knew I was sick but every DR said they didn't know until I got fat from pregnancy then it was Fibro since I was out of shape! They didn't believe I really was very thin before... I was just depressed from having the baby...blah… blah… blah...then the baby got sick with extreme GERD. They did test after test...I'm talking about putting a 3 month old out to do an upper GI and lower GI...they found nothing. Then at 15 mths Children’s Hospital GI Dr's said it was all psychological vomiting or rapid cycling vomiting but they couldn't officially could dx her with that until she was 5 yrs. They put her on meds that made her act nuts! She arched her back in pain. I mean she could not hold any formula or food down...up all night throwing up screaming in pain. We almost decided to get her stomach stapled. Glad I didn't!

This is long but worth it as it covers Lyme Facts and touches on all phases of this disease and different forms of treatment not just HBO

An Overview of Lyme Disease and
Hyperbaric Oxygen (HBO) Therapy

Mitchell L. Hoggard and L. James Johnson

Authors' Note:

This article is an overview of Lyme disease and hyperbaric oxygen (HBO) therapy. We acknowledge that the medical areas we explore can be complex and that any attempt to define and explain them in a way that is not overly technical can be incomplete and/or inadvertently confusing. We have attempted to be both clear and exact. Mitchell L. Hoggard is a pharmacist. He is also President and founder of the Chico Hyperbaric Center.

All three of his children have received HBO therapy for Lyme disease. Mitchell Hoggard's son Ted was 14 years old when he took part in William Fife's HBO research study on Lyme disease (more on the study later). L. James Johnson, formerly a broadcast journalist, is now a marketing consultant. He has received extensive HBO therapy for Lyme disease.

We have written this article to focus attention on what medical science knows and what it does not know about Lyme disease and HBO therapy. A lack of clarity in the diagnosis and treatment of Lyme disease has impacted both of our lives and the lives of our families. Also, this article was written to be supportive to a patient's relationship with their physician—not to take the place of that relationship.

Information on how to contact the authors follows this article.

Tom Grier is a microbiologist with a long time interest in Lyme
disease, he has written extensively about it, lectured and led a
support group and been on the board of directors of the Lyme Alliance
of Michigan (I believe the group is now defunct).

We are told by manufacturers, health departments and clinics that the
Lyme ELISA tests are good, useful tests, but in two blinded studies
that tested laboratories for accuracy, they failed miserably. Lorie
Bakken, MS/MPH, showed in her studies that there was not only
inaccuracy and inconsistency between competing laboratories, but also
between identical triple samples sent to the same lab. In other words,
identical samples often resulted in different results! In the first
study, forty-five labs correctly identified the samples only 55% of
the time.

In the latest study by the College of American Pathologists, 516 labs
were tested. The overall result was terrible! There were almost equal
numbers of false positives as false negatives. Overall, the labs were
55% inaccurate. The labs could only give a correct result 45% of the
time. YOU ARE ACTUALLY BETTER OFF TO FLIP A COIN!